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Titolo:
Anisodamine counteracts lipopolysaccharide-induced tissue factor and plasminogen activator inhibitor-1 expression in human endothelial cells: Contribution of the NF-kappa B pathway
Autore:
Ruan, QR; Zhang, WJ; Hufnagl, P; Kaun, C; Binder, BR; Wojta, J;
Indirizzi:
Univ Vienna, Dept Vasc Biol & Thrombosis Res, A-1090 Vienna, Austria Univ Vienna Vienna Austria A-1090 Thrombosis Res, A-1090 Vienna, Austria Tongji Med Univ, Dept Pathol, Tongji, Peoples R China Tongji Med Univ Tongji Peoples R China Pathol, Tongji, Peoples R China
Titolo Testata:
JOURNAL OF VASCULAR RESEARCH
fascicolo: 1, volume: 38, anno: 2001,
pagine: 13 - 19
SICI:
1018-1172(200101/02)38:1<13:ACLTFA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR NECROSIS FACTOR; SEPTIC SHOCK; ENDOTOXIN; INTERLEUKIN-1; PATHOGENESIS; BACTEREMIA; CACHECTIN; CYTOKINES; ANTIBODY; BIOLOGY;
Keywords:
anisodamine; lipopolysaccharide; endothelial cells; plasminogen activator inhibitor-1; tissue factor; NF-kappa B;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Wojta, J Univ Vienna, Dept Internal Med 2, Waehringer Guertel 18-20, A-1090 Vienna,Austria Univ Vienna Waehringer Guertel 18-20 Vienna Austria A-1090 stria
Citazione:
Q.R. Ruan et al., "Anisodamine counteracts lipopolysaccharide-induced tissue factor and plasminogen activator inhibitor-1 expression in human endothelial cells: Contribution of the NF-kappa B pathway", J VASC RES, 38(1), 2001, pp. 13-19

Abstract

In this study we aimed to investigate whether the therapeutic efficacy of anisodamine in the treatment of bacteraemic shock could - at least in part - be brought about by its direct interference with the lipopolysaccharide (LPS)-induced activation of endothelial cells. Thus, we investigated the effect of anisodamine on LFS-induced expression of plasminogen activator inhibitor-1 (PAI-1) and tissue factor (TF), two major markers of endothelial activation. PAI-1 was measured in the conditioned media of human umbilical vein endothelial cells (HUVEC) by a specific enzyme-linked immunosorbent assay(ELISA) whereas TF activity was measured in the lysates of these cells by using a single step clotting assay. Results obtained in these assays were confirmed on the level of specific mRNA expression by Northern blotting using specific probes for human PAI-1 or TF. In order to evaluate a possible contribution of the NF-kappaB pathway on the effects observed, electrophoretic mobility shift assays (EMSA) were performed using nuclear extracts from HUVEC and NF-kappaB-binding oligonucleotides. When HUVEC were treated with 1mug/ml LPS a significant increase in PAI-1 and TF activity was observed compared with cells incubated without LPS. Anisodamine dose-dependently inhibited this LPS-induced upregulation of PAI-1 and TF. Anisodamine alone had no effect on the constitutive expression of PAI-1 and TF in these cells. These effects were also confirmed on the level of specific PAI-1 and TF mRNA expression by Northern blotting. Furthermore, we could show by EMSA that anisodamine completely abolished LPS-induced NF-kappaB DNA binding activity innuclear extracts from HUVEC treated with LPS together with anisodamine. Thus, we provide evidence that anisodamine counteracts endothelial cell activation by inhibiting LPS-induced PAI-1 and TF expression in these cells. Itsinterference with the NF-kappaB pathway might - at least in pa rt - contribute to th is effect. The ability of an isodamine to counteract LPS effectson endothelial cells might be one underlying mechanism explaining its efficacy in the treatment of bacteraemic shock. Copyright (C) 2001 S. Karger AG, Basel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 07:24:08